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Effects of GABAergic transmissions on the immunoreactivities of calcium binding proteins in the gerbil hippocampus

✍ Scribed by Sung-Eun Kwak; Ji-Eun Kim; Duk-Soo Kim; Ju-Young Jung; Moo Ho Won; Oh-Shin Kwon; Soo-Young Choi; Tae-Cheon Kang

Publisher: John Wiley and Sons
Year: 2005
Tongue: English
Weight: 827 KB
Volume: 485
Category: Article
ISSN: 0021-9967
DOI: 10.1002/cne.20482

No coin nor oath required. For personal study only.

✦ Synopsis

Although reduced calcium binding protein (CBP) immunoreactivities in the epileptic hippocampus have been well established, it has been controversial that these changes may directly indicate neuronal degeneration. In the present study, therefore, we investigated CBP expressions in the gerbil hippocampus following treatment with ␥-aminobutyric acid (GABA) receptor antagonists in order to assess whether altered CBP expressions are the result of either abnormal excitation or indicative of neuronal damage/degeneration. Seizure-sensitive (SS) gerbils showed a loss/decline of CBP immunoreactivities in some hippocampal neurons as compared with seizure-resistant (SR) gerbils. In muscimol (GABA A receptor agonist) treated SS gerbils, expression levels of CBP were enhanced as compared with saline-treated SS gerbils. Bicuculline (a GABA A receptor antagonist) treatment markedly reduced CBP immunoreactivities in hippocampal neurons of the SR gerbil. Baclofen (a GABA B receptor agonist) treatment increased CBP immunoreactivities in the hippocampus of SS gerbils, although its effect was lower than that of muscimol treatment. Moreover, phaclofen (GABA B receptor antagonist) treated SR gerbil showed reduction in calbindin D-28K immunoreactivity, not parvalbumin immunoreactivity, in the hippocampus. These findings therefore suggest that reduced CBP immunoreactivities may be the consequence of abnormal discharge caused by loss of GABAergic inhibition rather than an indication of the neuronal damage/ degeneration.

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